Antipsychotics Lower Peripheral Markers of Inflammation in Drug-naïve Early Psychosis: A Pilot Study
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Introduction
Neuroinflammation is increasingly recognized as a core pathophysiological mechanism in schizophrenia and can be indirectly assessed through peripheral inflammatory markers. Therefore, this pilot study investigated the impact of antipsychotic treatment on inflammation in patients with first-episode psychosis (FEP) who were antipsychotic-naive at study entry.
Methods
Thirty-three drug-naïve FEP patients provided blood samples upon admission (V0) and follow-up (V1), from which inflammatory markers—i.e., neutrophil/lymphocyte ratio (NLR), monocyte/lymphocyte ratio (MLR), platelet/lymphocyte ratio (PLR), and systemic immune-inflammation index (SII)—were calculated. Antipsychotic doses during continuous hospitalization between V0 and V1 (37.21 ± 19.85 days) were converted into cumulative chlorpromazine equivalents (cCHPMZ). Linear regression models correlated cCHPMZ with changes in markers, adjusting for sex, age, duration of untreated psychosis (DUP), and clozapine use.
Results
Higher cCHPMZ was significantly associated with reductions in NLR ( p = 0.029), MLR ( p = 0.016), PLR ( p = 0.016), and SII ( p = 0.010). Male sex predicted an increase in MLR ( p = 0.026). After the Benjamini-Hochberg FDR correction, these associations remained significant (FDR < 0.05). Although clozapine use and DUP were not significant predictors, they slightly improved the model fit for PLR, SII, and MLR, respectively, as indicated by reductions in AIC and RSE values. Age did not predict changes in inflammatory markers in any of the models.
Conclusion
The observed correlation between cumulative antipsychotic exposure and reductions in hematologic inflammatory markers suggests that antipsychotics may exert anti-inflammatory effects, potentially in a dose-related manner. Larger studies are needed to confirm this and clarify the role of inflammation in schizophrenia pathophysiology.
